THIS IS AN ONLINE E LOG BOOK TO DISCUSS OUR PATIENT'S DE-IDENTIFIED HEALTH DATA SHARED AFTER TAKING HIS SIGNED INFORMED CONSENT. HERE WE DISCUSS OUR PATIENT'S PROBLEMS THROUGH SERIES OF INPUTS FROM AVAILABLE GLOBAL ONLINE COMMUNITY EXPERTS WITH AN AIM TO SOLVE THOSE PATIENT'S CLINICAL PROBLEMS WITH COLLECTIVE CURRENT BEST EVIDENCE BASED INPUTS.
[23-05-2025 12.23] PPM 1: 40M regular alcohol consumer, trunkal obesity, diabetes and Hypertension since 3 years, had a sudden quadriparesis three years back but recovered soon and then continued drinking and having weakness as well as slurred speech which was difficult to differentiate if it was from drinking or some other focal neurological deficit! 6 days back had a sudden left hemiparesis waking up in the morning following which recovered completely after reaching hospital in two hours but it struck again after few hours and he has been left hemiparetic since the last 6 days!
https://youtu.be/BM_xNWi9zSA?si=rj6nruQepuuY0LxK
[23-05-2025 12:42] PPM 1: They were referred from Ibrahimpatnam near Hyderabad and chose to come to our hospital instead of Osmania in the heart of Hyderabad! They changed 4 autos across 100 kms to reach our OPD today! @PPM4
[23-05-2025 12:44] PPM 3: Thank you for the detailed clinical background and the CT scan image. Here's a comprehensive interpretation and synthesis:
---
### 🧠 *Clinical Summary*:
*40M with multiple vascular risk factors*:
* Long-standing *diabetes mellitus, **hypertension, **chronic alcohol use, and **truncal obesity*
* History of:
* *Past quadriparesis (transient)* — 3 years ago
* *Persistent weakness + slurred speech*
* *Recent episode (6 days ago): Sudden **left hemiparesis*, resolved then recurred → persistent deficit since
This pattern strongly suggests *recurrent cerebrovascular events*, likely of ischemic etiology.
---
### 🧠 *CT Brain Interpretation*:
On non-contrast axial CT scan:
* *Hypodensity* in the *right internal capsule and corona radiata region* is evident → correlates with *left hemiparesis*.
* Chronic *periventricular and subcortical white matter hypodensities* suggestive of *chronic small vessel ischemic changes*.
* *Ex vacuo dilatation of lateral ventricles* due to surrounding parenchymal volume loss — likely chronic.
* No signs of hemorrhage, midline shift, or mass effect in current slices.
---
### 🧠 *Working Diagnosis*:
> *Recurrent Ischemic Stroke (Subcortical Lacunar Infarct)* involving the *right internal capsule/corona radiata, likely due to **small vessel disease* (hypertensive and diabetic arteriopathy).
Contributory pathology may include:
* *Alcohol-related nutritional deficiency* (e.g., thiamine) → could have caused prior encephalopathy or subtle deficits.
* *Possible prior transient ischemic attacks (TIAs)* – explained by fluctuating past symptoms.
---
### 🔍 Suggested Work-up:
* *MRI Brain with DWI/FLAIR*: For better characterization of acute vs chronic infarcts.
* *MRA or CTA Head/Neck*: To rule out large-vessel pathology or tandem stenosis.
* *Echocardiography + ECG + 24h Holter*: Cardioembolic source?
* *HbA1c, Lipid panel, Liver function tests, **vitamin B1 (thiamine), **folate, **B12*.
* *Neuropsychological assessment* for cognitive deficits masked by alcohol use.
---
### 🧠 Final Impression:
*Case of recurrent lacunar strokes* in the setting of *metabolic syndrome* and *chronic alcohol use, with probable **strategic infarcts* leading to persistent deficits.
Would you like this formalized into a discharge summary or ward round note?
Scholar
[23-05-2025 12:49] PPM 3: The patient's clinical presentation and history suggest recurrent cerebrovascular events, likely ischemic strokes, in the context of multiple vascular risk factors (hypertension, diabetes, obesity, chronic alcohol use). Here's a structured analysis:
### *Key Clinical Features:*
1. *Recurrent Neurological Deficits:*
- *Three years ago:* Sudden quadriparesis (resolved quickly) → suggestive of a vertebrobasilar TIA or stroke.
- *Recent episode:* Left hemiparesis (initially transient, then persistent) → points to right middle cerebral artery (MCA) territory ischemia.
2. *Risk Factors:* Hypertension, diabetes, trunkal obesity, chronic alcohol use (increases stroke risk via cardiomyopathy, arrhythmias, hypertension, and hypercoagulability).
3. *Alcohol-Related Complications:* Slurred speech and chronic weakness may reflect cerebellar degeneration, neuropathy, or prior strokes.
---
### *Differential Diagnosis:*
1. *Ischemic Stroke:*
- *Embolic Source:* Atrial fibrillation (alcohol-induced cardiomyopathy), carotid stenosis, or cardioembolism.
- *Small Vessel Disease:* Hypertension/diabetes causing lacunar strokes (less likely with hemiparesis).
- *Cryptogenic Stroke:* Hypercoagulability or undetected cardioembolic source.
2. *Hemorrhagic Stroke:* Less likely without acute headache/coma, but chronic hypertension increases risk.
3. *Other Considerations:*
- *Subdural Hematoma:* Possible if history of falls (alcohol-related), but no trauma reported.
- *Metabolic (e.g., hypoglycemia, Wernicke’s):* Unlikely with persistent deficits.
- *Seizure (Todd’s paralysis):* Brief deficits, but recurrence/persistence atypical.
---
### *Urgent Workup:*
1. *Neuroimaging:*
- *Non-contrast CT Head:* Rule out hemorrhage.
- *MRI Brain with DWI:* Confirm acute ischemia, assess vascular territories (e.g., right MCA for left hemiparesis; prior vertebrobasilar lesions).
- *Vascular Imaging (CTA/MRA):* Evaluate carotid/vertebral arteries, intracranial stenosis.
2. *Cardiac Evaluation:*
- *EKG/24-hour Holter:* Detect atrial fibrillation.
- *Echocardiogram:* Assess for cardiomyopathy, valvular disease, thrombus.
3. *Laboratory Tests:*
- Glucose, lipid panel, HbA1c, renal/liver function, coagulation studies.
- Toxicology screen (if illicit drug use suspected).
- Thiamine (given alcohol history).
---
### *Management:*
1. *Acute Stroke Care:*
- *Beyond thrombolysis window* (6 days since onset), focus on secondary prevention.
2. *Secondary Prevention:*
- *Antiplatelets:* Aspirin + clopidogrel (short-term dual therapy if recent TIA/stroke) or monotherapy.
- *Anticoagulation:* If atrial fibrillation is detected (e.g., direct oral anticoagulants).
- *Risk Factor Control:*
- Strict BP control (target <130/80 mmHg).
- Diabetes management (HbA1c <7%).
- High-intensity statin (e.g., atorvastatin 40-80 mg).
- *Alcohol Cessation:* Critical to reduce recurrence risk.
3. *Rehabilitation:* Physical/occupational therapy for residual hemiparesis.
---
### *Conclusion:*
The patient likely experienced recurrent ischemic strokes due to embolic or atherothrombotic mechanisms. A cardioembolic source (e.g., atrial fibrillation) must be ruled out. Urgent neuroimaging and vascular/cardiac workup are essential to guide therapy. Long-term management hinges on aggressive risk factor modification and alcohol cessation.{DeepSeek(withoutsharingtheCTscanimage)}
[23-05-2025 22.12] PPM 3: Skip to main content
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This is a complex case with multiple concerning features. The patient has significant vascular risk factors and a history suggestive of recurrent neurological events.
Summary of Key Points:
40M, chronic alcohol consumer, truncal obesity, DM, HTN (all for 3 years).
3 years ago: Sudden quadriparesis, recovered soon.
Ongoing since then: Weakness, slurred speech (confounded by alcohol).
6 days ago:
Woke with sudden left hemiparesis.
Complete recovery in hospital within 2 hours (suggestive of a Transient Ischemic Attack - TIA).
Recurrence of left hemiparesis a few hours later, persistent for the last 6 days (suggestive of an acute ischemic stroke).
Most Likely Diagnosis for the Current Event:
Acute Ischemic Stroke in the right cerebral hemisphere (e.g., right Middle Cerebral Artery - MCA territory, or lacunar stroke in the internal capsule/pons). The initial transient event followed by a persistent deficit is highly characteristic of a "stuttering stroke" or a TIA followed by a completed stroke.
Differential Diagnoses for the Current Event (and consideration of past events):
Ischemic Stroke (Cerebrovascular Accident - CVA):
Etiology:
Large artery atherosclerosis: Given HTN, DM, obesity, and alcohol, stenosis/occlusion of carotid arteries or intracranial arteries (e.g., MCA) is highly probable. The stuttering course can be due to fluctuating perfusion or recurrent emboli from an unstable plaque.
Small vessel disease (Lacunar infarct): Due to chronic HTN and DM. Could explain the current hemiparesis and potentially the prior quadriparesis (e.g., bilateral pontine lacunes).
Cardioembolism: Alcohol can contribute to atrial fibrillation (even paroxysmal) or alcoholic cardiomyopathy. An echocardiogram would be crucial.
Other: Dissection (less likely without trauma history), vasculitis (rare).
Location of current stroke: Right MCA territory, right internal capsule, right corona radiata, or right brainstem (pons).
Intracerebral Hemorrhage (ICH):
Hypertension is a major risk factor. Alcohol can also contribute to coagulopathy or increase risk.
Sudden onset is typical. A non-contrast CT brain would have been the first imaging done in the hospital to rule this out. If the recovery was truly complete after the first event, hemorrhage is less likely for that specific transient episode, but could be the cause of the persistent deficit.
Regarding the previous Quadriparesis (3 years ago):
Bilateral Ischemic Strokes: Could have been bilateral watershed infarcts or multiple lacunar infarcts in strategic locations (e.g., bilateral internal capsules, brainstem).
Brainstem Stroke: A single lesion in the pons or medulla could cause quadriparesis.
Spinal Cord Event: Less likely with rapid recovery and subsequent focal cerebral events, but consider vascular myelopathy or even an inflammatory cause at the time (e.g., transverse myelitis, though recovery pattern is atypical).
Metabolic/Toxic:
Osmotic Demyelination Syndrome (Central Pontine Myelinolysis): Can occur with rapid correction of hyponatremia, sometimes seen in alcoholics. Can cause quadriparesis and dysarthria. Recovery can be variable.
Severe Hypokalemic Periodic Paralysis: Though usually episodic and related to triggers, and less likely to be "sudden" in this context without a clear precipitant.
Wernicke's Encephalopathy (severe variant): While classical triad is ataxia, ophthalmoplegia, confusion, severe cases can present with profound weakness. Thiamine deficiency is common in alcoholics.
Ongoing weakness and slurred speech:
Residual deficits from the previous quadriparetic event.
Chronic effects of alcohol: Cerebellar degeneration (ataxia, dysarthria), alcoholic neuropathy (weakness), alcoholic myopathy.
This makes assessing new focal deficits more challenging.
Immediate Management (What should have happened and what is needed now):
Neuroimaging (If not already comprehensively done):
Non-Contrast CT Brain: To rule out hemorrhage (should have been done immediately upon presentation).
MRI Brain (with DWI, ADC, FLAIR, GRE/SWI sequences): Gold standard for confirming acute ischemic stroke, defining its extent, and identifying old infarcts or microbleeds.
MRA (Magnetic Resonance Angiography) of Head and Neck OR CT Angiography (CTA): To assess for large vessel stenosis/occlusion in carotids, vertebrals, and intracranial arteries.
Basic Labs:
CBC, electrolytes, renal function, liver function tests (LFTs - important due to alcohol).
Coagulation profile (PT/INR, aPTT).
Fasting blood glucose and HbA1c.
Lipid profile.
Thiamine levels (if Wernicke's or ODS is suspected for past events).
Cardiac Workup:
ECG: To look for atrial fibrillation or signs of ischemia.
Echocardiogram (Transthoracic, possibly Transesophageal - TEE): To rule out cardioembolic source (PFO, valvular disease, LV thrombus, atrial thrombus, cardiomyopathy).
Consider Holter monitoring if paroxysmal AFib is suspected.
Management Plan (Since he is 6 days post-stroke):
Confirmation of Diagnosis: Ensure ischemic stroke is confirmed and hemorrhage ruled out by imaging.
Secondary Stroke Prevention (Crucial):
Antiplatelet Therapy: Aspirin, Clopidogrel, or Aspirin + Dipyridamole. Dual antiplatelet therapy (Aspirin + Clopidogrel) might be considered for a short period (e.g., 21-90 days) depending on stroke subtype and local guidelines, especially if high-risk TIA or minor stroke due to large artery atherosclerosis.
Statin Therapy: High-intensity statin (e.g., Atorvastatin 80mg or Rosuvastatin 40mg) regardless of baseline cholesterol levels.
Blood Pressure Management: Target BP <130/80 mmHg (or as per guidelines).
Diabetes Management: Strict glycemic control, target HbA1c <7%.
Lifestyle Modification:
Absolute Alcohol Cessation: This is paramount. Provide counseling, support, and consider medications for alcohol use disorder. Thiamine supplementation is essential.
Dietary changes: Low salt, low saturated fat, focus on fruits, vegetables, whole grains.
Weight management: Aim for healthy BMI.
Regular physical activity: As tolerated and guided by rehabilitation.
Rehabilitation:
Physiotherapy: For hemiparesis, mobility, balance.
Occupational Therapy: For activities of daily living.
Speech and Language Therapy: For dysarthria (slurred speech) and swallow assessment (dysphagia risk).
Management of Complications:
DVT Prophylaxis: (e.g., LMWH if immobile, compression stockings).
Swallow Assessment: To prevent aspiration pneumonia. NGT/PEG if necessary.
Monitoring for: Pressure sores, infections (UTI, pneumonia), depression.
Addressing the "Quadriparesis 3 years ago": If not fully investigated, previous imaging should be reviewed or new imaging (e.g., MRI spine if indicated) might be considered depending on the full clinical picture and to understand the overall burden of neurological disease.
Prognosis:
The prognosis is guarded due to:
Multiple uncontrolled vascular risk factors.
Recurrent neurological events, suggesting aggressive underlying disease.
Continued alcohol consumption, which exacerbates risks and can cause direct neurotoxicity.
The current persistent hemiparesis indicates a significant stroke.
Aggressive risk factor modification, especially alcohol cessation, and adherence to secondary prevention strategies are critical to prevent further devastating events. The degree of recovery from the current hemiparesis will depend on the size and location of the infarct and the intensity of rehabilitation.
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